Evaluation of the frequency of Helicobacter pylori infection and atrophic gastritis in patients diagnosed with celiac disease

Abstract

Aim: Celiac disease (CD) is a chronic inflammatory enteropathy triggered by an autoimmune response to gluten. This study aimed to determine gastric pathologies accompanying CD, with a focus on the frequency of Helicobacter pylori (H. pylori) infection and atrophic gastritis. Material and Methods: Between January 2010 and March 2018, 47 patients diagnosed with CD at the Gastroenterology Clinic of Kayseri Training and Research Hospital, who underwent gastric biopsy during endoscopy, were enrolled as the study group. The control group consisted of 47 age- and gender-matched patients who underwent endoscopy for dyspeptic complaints. The groups were compared regarding the presence of atrophic gastritis, H. pylori, lymphocytic gastritis, and intestinal metaplasia. Data were analyzed using IBM SPSS V23. Results: A total of 94 patients (47 CD, 47 dyspepsia) were included. Both groups comprised 20 male and 27 female patients. Atrophy frequency was 27.7% in the CD group and 17.0% in the dyspepsia group (p = 0.322). H. pylori positivity was 61.7% in the CD group and 74.5% in the dyspepsia group (p = 0.269). Lymphocytic gastritis was present in 12.8% of the CD group but was not detected in the control group (p = 0.011). No statistical difference was found in metaplasia frequency (p = 0.307). Serum vitamin B12 levels were below 200 pg/mL in 80% of CD patients. Conclusion: Gastric biopsy during endoscopy is recommended for celiac patients, particularly those with persistent anemia, dyspepsia, or B12 deficiency despite a gluten-free diet. While the frequencies of H. pylori infection and atrophic gastritis were similar to those in the control group, lymphocytic gastritis was significantly more common in CD patients. This finding underscores the importance of evaluating gastric mucosal changes to manage refractory symptoms and nutritional deficiencies effectively.

Keywords

• celiac disease
• helicobacter pylori
• atrophic gastritis
• lymphocytic gastritis
• Vitamin B12

Ethical Statement

The study was approved by the Medical Specialization Education Board of the University of Health Sciences Kayseri Training and Research Hospital (Decision No: 13, dated March 20, 2018).

Çölyak hastalığı tanılı hastalarda Helicobacter pylori enfeksiyonu ve atrofik gastrit sıklığının değerlendirilmesi

Abstract

Amaç: Çölyak hastalığı (ÇH), glutene karşı gelişen otoimmün yanıtın tetiklediği kronik inflamatuar bir enteropatidir. Bu çalışmada, ÇH’ye eşlik eden gastrik patolojilerin belirlenmesi, özellikle Helicobacter pylori (H. pylori) enfeksiyonu ve atrofik gastrit sıklığının saptanması amaçlanmıştır. Gereç ve Yöntemler: Ocak 2010 ile Mart 2018 tarihleri arasında Kayseri Eğitim ve Araştırma Hastanesi Gastroenteroloji Kliniği’nde ÇH tanısı alan ve endoskopi sırasında gastrik biyopsi yapılan 47 hasta çalışma grubuna dahil edildi. Kontrol grubu, dispeptik şikayetler nedeniyle endoskopi yapılan benzer yaş ve cinsiyetteki 47 hastadan oluşturuldu. Gruplar; atrofik gastrit, H. pylori, lenfositik gastrit ve intestinal metaplazi varlığı açısından karşılaştırıldı. Veriler IBM SPSS V23 kullanılarak analiz edildi. Bulgular: Toplam 94 hasta (47 ÇH, 47 dispepsi) çalışmaya dahil edildi. Her iki grupta da 20 erkek ve 27 kadın hasta mevcuttu. Atrofi sıklığı ÇH grubunda %27,7, dispepsi grubunda ise %17,0 olarak saptandı (p = 0,322$). H. pylori pozitifliği ÇH grubunda %61,7 iken kontrol grubunda %74,5 idi (p = 0,269$). Lenfositik gastrit ÇH grubunda %12,8 oranında görülürken, kontrol grubunda saptanmadı (p = 0,011$). Metaplazi sıklığında istatistiksel fark bulunmadı (p = 0,307$). ÇH hastalarının %80’inde serum vitamin B12 düzeyleri 200 pg/mL'nin altında saptandı. Sonuç: Çölyak hastalarında, özellikle glutensiz diyete rağmen persistan anemi, dispepsi veya B12 eksikliği olanlarda endoskopi sırasında gastrik biyopsi yapılması önerilir. H. pylori enfeksiyonu ve atrofik gastrit sıklığı kontrol grubuyla benzer olsa da lenfositik gastrit ÇH hastalarında anlamlı derecede daha yaygındır. Bu bulgu, dirençli semptomların ve beslenme yetersizliklerinin etkin yönetimi için gastrik mukoza değişikliklerinin değerlendirilmesinin önemini vurgulamaktadır.

Keywords

• çölyak hastalığı
• helicobacter pylori
• atrofik gastrit
• lenfositik gastrit
• vitamin B12.

References

1. Green PH, Cellier C. Celiac disease. N Engl J Med. 2007; 357: 1731–43.
2. Fasano A. Clinical presentation of celiac disease in the pediatric population. Gastroenterology. 2005; 128: S68-S73.
3. Biagi F, Trotta L, Alfano C, Balduzzi D, Staffieri V, Bianchi PI, et al. Prevalence and natural history of potential celiac disease in adult patients. Scand J Gastroenterol. 2013; 48: 537-42.
4. Rugge M, Genta RM. Staging and grading of chronic gastritis. Hum Pathol. 2005; 36: 228-33.
5. Lebwohl B, Sanders DS, Green PHR. Coeliac disease. Lancet. 2018; 391: 70-81.
6. Villanacci V, Bassotti G, Liserre B, Lanzini A, Lanzarotto F, Genta RM. Helicobacter pylori infection in patients with celiac disease. Am J Gastroenterol. 2006; 101: 1880-5.
7. Villanacci V, Vanoli A, Leoncini G, Arpa G, Salviato T, Bonetti LR, et al. Celiac disease: histology-differential diagnosis- complications. A practical approach. Pathologica. 2020; 112: 186-96.
8. Parsonnet J, Friedman GD, Vandersteen DP, Chang Y, Vogelman JH, Orentreich N, Sibley RK. Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med. 1991; 325: 1127-31.

9. Centanni M, Marignani M, Gargano L, Corleto VD, Casini A, Delle Fave G, et al. Atrophic body gastritis in patients with autoimmune thyroid disease: an underdiagnosed association. Arch Intern Med.1999; 159: 1726-30.
10. Ozçay F, Koçak N, Temizel IN, Demir H, Ozen H, Yüce A, Gürakan F. Helicobacter pylori infection in Turkish children: comparison of diagnostic tests, evaluation of eradication rate, and changes in symptoms after eradication. Helicobacter. 2004; 9: 242-8.
11. Fayed SB, Aref MI, Fathy HM, Abd El Dayem SM, Emara NA, Maklof A, Shafik A. Prevalence of celiac disease, Helicobacter pylori and gastroesophageal reflux in patients with refractory iron deficiency anemia. J Trop Pediatr. 2008; 54: 43-53.
12. Ciacci C, Squillante A, Rendina D, Limauro S, Bencivenga C, Labanca F, et al. Helicobacter pylori infection and peptic disease in coeliac disease. Eur J Gastroenterol Hepatol. 2000; 12: 1283-7.
13. Kakar S, Nehra V, Murray JA, Dayharsh GA, Burgart LJ. Significance of intraepithelial lymphocytosis in small bowel biopsy samples with normal mucosal architecture. Am J Gastroenterol. 2003; 98: 2027-33.
14. Schuppan D, Zimmer KP. The diagnosis and treatment of celiac disease. Dtsch Arztebl Int. 2013; 110: 835-46.
15. Konturek PC, Konturek SJ, Brzozowski T. Helicobacter pylori infection in gastric cancerogenesis. J Physiol Pharmacol. 2009; 60: 3-21.
16. Basyigit S, Unsal O, Uzman M, Sapmaz F, Dogan OC, Kefeli A, et al. Relationship between Helicobacter pylori infection and celiac disease: a cross-sectional study and a brief review of the literature. Prz Gastroenterol. 2017; 12: 49-54.
17. Kahramanoğlu Aksoy E, Sapmaz F, Akpınar MY, Uzman M, Göktaş Z. Çölyak hastalığında Helicobacter pylori prvelansının değerlendirilmesi. Akadamik Gastroenteroloji Dergisi 2018; 17: 12-6.
18. Coeliac Disease: Recognition, Assessment and Management. London: National Institute for Health and Care Excellence (NICE); 2015 Sep. (NICE Guideline, No. 20.) Appendix F, Excluded studies. Available from: https:// www.ncbi.nlm.nih.gov/books/NBK343367/
19. O'Leary C, Walsh CH, Wieneke P, O'Regan P, Buckley B, O'Halloran DJ, et al. Coeliac disease and autoimmune Addison's disease: a clinical pitfall. QJM. 2002; 95: 79-82.